Wave propagation of myocardial stretch: Correlation with myocardial stiffness

The mechanism of flow propagation during diastole in the left ventricle (LV) has been well described. Little is known about the associated waves propagating along the heart walls. These waves may have a mechanism similar to pulse wave propagation in arteries. The major goal of the study was to evaluate the effect of myocardial stiffness and preload on this wave transmission. Longitudinal late diastolic deformation and wave speed (Vp) of myocardial stretch in the anterior LV wall were measured using sonomicrometry in 16 pigs. Animals with normal and altered myocardial stiffness (acute myocardial infarction) were studied with and without preload alterations. Elastic modulus estimated from Vp (E_VP; Moens–Korteweg equation) was compared to incremental elastic modulus obtained from exponential end-diastolic stress–strain relation (E_SS). Myocardial distensibility and α- and β-coefficients of stress–strain relations were calculated. Vp was higher at reperfusion compared to baseline (2.6 ± 1.3 vs. 1.3 ± 0.4 m/s; p = 0.005) and best correlated with E_SS (r² = 0.80, p < 0.0001), β-coefficient (r² = 0.78, p < 0.0001), distensibility (r² = 0.47, p = 0.005), and wall thickness/diameter ratio (r² = 0.42, p = 0.009). Elastic moduli (E_VP and E_SS) were strongly correlated (r² = 0.83, p < 0.0001). Increasing preload increased Vp and E_VP and decreased distensibility. At multivariate analysis, E_SS, wall thickness, and end-diastolic and systolic LV pressures were independent predictors of Vp (r² model = 0.83, p < 0.0001). In conclusion, the main determinants of wave propagation of longitudinal myocardial stretch were myocardial stiffness and LV geometry and pressure. This local wave speed could potentially be measured noninvasively by echocardiography.